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Lactate supplementation in severe traumatic brain injured adults by primed constant infusion of sodium L-lactate.
Wolahan, Stephanie M; Mao, Howard C; Real, Courtney; Vespa, Paul M; Glenn, Thomas C.
Afiliação
  • Wolahan SM; UCLA Brain Injury Research Center and the Department of Neurosurgery, David Geffen School of Medicine at UCLA, University of California-Los Angeles, Los Angeles, California, USA.
  • Mao HC; UCLA Brain Injury Research Center and the Department of Neurosurgery, David Geffen School of Medicine at UCLA, University of California-Los Angeles, Los Angeles, California, USA.
  • Real C; UCLA Brain Injury Research Center and the Department of Neurosurgery, David Geffen School of Medicine at UCLA, University of California-Los Angeles, Los Angeles, California, USA.
  • Vespa PM; UCLA Brain Injury Research Center and the Department of Neurosurgery, David Geffen School of Medicine at UCLA, University of California-Los Angeles, Los Angeles, California, USA.
  • Glenn TC; UCLA Brain Injury Research Center and the Department of Neurosurgery, David Geffen School of Medicine at UCLA, University of California-Los Angeles, Los Angeles, California, USA.
J Neurosci Res ; 96(4): 688-695, 2018 04.
Article em En | MEDLINE | ID: mdl-28543565
ABSTRACT
Carbohydrate fuel augmentation following traumatic brain injury may be a viable treatment to improve recovery when cerebral oxidative metabolism of glucose is depressed. We performed a primed constant sodium L-lactate infusion in 11 moderate to severely brain injured adults. Blood was collected before and periodically during the infusion study. We quantified global cerebral uptake of glucose and lactate and other systemic metabolites associated with energy metabolism. Our hypothesis was that cerebral lactate uptake, as measured by the arteriovenous difference of lactate (AVDlac), would increase in severely injured TBI patients in the neurocritical care unit. Infusion of sodium L-lactate changed net cerebral lactate release, where the arteriovenous difference of lactate is negative, to net cerebral lactate uptake. Results from a mixed effects model of AVDlac with the fixed effects of infusion time, arterial lactate concentration, arterial glucose concentration and arteriovenous difference of glucose shows that doubling arterial lactate concentration (from .92 to 1.84 mM) results in an increase in AVDlac from -.078 mM to .090 mM. We did not detect changes in systemic glucose during the course of the infusion study and observed significant changes in alanine (30% [20 39]), glutamine (34% [24 43]), acetate (87% [60 113]), valine (40% [28 51]), and leucine (24% [16 32]) from baseline levels. Further studies are required to establish the impact of lactate supplementation on cerebral and systemic flux of lactate, on gluconeogenesis, and on the impact on cerebral energetics following injury. © 2017 Wiley Periodicals, Inc.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Ácido Láctico / Lactato de Sódio / Lesões Encefálicas Traumáticas Idioma: En Ano de publicação: 2018 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Ácido Láctico / Lactato de Sódio / Lesões Encefálicas Traumáticas Idioma: En Ano de publicação: 2018 Tipo de documento: Article